Cardio Flashcards

Question

SVT: AV Reciprocating Tachycardia (AVRT) defintion, sx, dx, tx

Answer 1

*HR 140-250bpm, ectopic P wave; sudden onset/termination *reentry mechanism via bypass tract between atria/ventricles, risk of VFIB *only 5-10% of pts w/ bypass tracts have structural disease (Ebstein anomaly MC) S/SXS: varies; palpitations, diaphoresis, SOB, dizziness, CP – syncope rare PATHO: tachycardia usually initiated by PAC/PVC; reentry circuit develops *Orthodromic (MC): anterograde over AV node, retrograde over accessory pathway *NARROW QRS, retrograde P wave after QRS *Antidromic: anterograde over accessory pathway, retrograde over AV node *WIDE QRS, ⊕DELTA WAVE, P wave rare (retrograde before QRS if visible) dx *Orthodromic: narrow QRS, retrograde P wave after QRS, ⊖delta wave *Antidromic: wide QRS, ⊕ delta wave, P wave rarely visible tx Asymptomatic w/ ⊕ delta wave: *generally don’t require treatment *vagal maneuvers – Valsalva, carotid massage *IV adenosine almost always works *AVN blocking agents (BBs, CCBs, digoxin) Refractory: catheter ablation

Answer 2

*≥3 ectopic atrial foci generating impulses that are all conducted to the ventricles *irregularly irregular rhythm w/ varying PR intervals Wandering Atrial Pacemaker (“multifocal atrial rhythm”) = HR ≤100bpm Multifocal Atrial Tachycardia = HR >100bpm – MAT associated w/ COPD! – hypoxia, electrolyte abnormalities (e.g., hypokalemia, hypomagnesemia) dx EKG: ≥3 distinct P wave morphologies in the same lead ▪︎irregularly irregular rhythm, varying PP/PR/RR intervals ▪isoelectric line between P waves (i.e., ⊘flutter waves) Wandering Atrial Pacemaker: HR ≤100bpm Multifocal Atrial Tachycardia (MAT): HR >100bpm tx WAP: benign, requires no treatment Pharmacotherapy for MAT indicated if: – Leads to sustained RVR that causes or worsens myocardial ischemia, HF, peripheral perfusion, or oxygenation *Verapamil: COPD (d/t bronchospasm) *Metoprolol – AADs & cardioversion NOT usefulWolff-Parkinson White (WPW)

Answer 3

WPW Pattern: EKG findings w/o symptomatic arrhythmias WPW Syndrome: congenital accessory pathway (Bundle of Kent) w/ associated SVT S/SXS: if ⊕arrhythmia, may have palpitations, dizziness, or mild chest pain dx WPW: ➀ ⊕delta wave ➁ short PR interval (<120ms) ➂ wide QRS (>110ms) ▪︎secondary ST-T changes AFIB in WPW: rate >200bpm, irregularly irregular rhythm » occasional narrow QRS reflects AV node conduction » wide QRS d/t anterograde conduction through accessory pathway (rates close to 300bpm) tx Narrow complex tachycardia: *implies conduction over AV node *treat similar to AVNRT Wide complex tachycardia: *implies conduction over accessory path – AVOID AVN-blocking agents *may precipitate VFIB – unstable: electrical cardioversion – stable: IV procainamide or ibutilide TOC: electrophysiologic study & catheter ablation of bypass tracts

Answer 4

*typically a normal variant dx EKG Findings: premature beat followed by a normal QRS, P wave has different morphology from sinus P wave S/SXS: +/- palpitations tx usually no treatment required Complications: atrial tachycardia, AFIB/flutter

Answer 5

*occasional PVCs occur in healthy adults Other causes: *stimulants (e.g., caffeine, nicotine, cocaine) *catecholamine surge (e.g., pain), ischemia *electrolyte abnormalities (e.g., hypokalemia) *medication toxicity dx EKG Findings: premature wide QRS w/o preceding P wave *followed by fully compensatory pause (interval between sinus beats before/after PVC is 2 RR intervals) *≥3 PVCs = nonsustained VTACH S/SXS: +/- palpitations TX: usually no treatment required. can give BB

Answer 6

VT: ≥3 consecutive PVCs – Nonsustained: lasts <30s & terminates spontaneously – Sustained: no spontaneous termination, >100bpm MCC: acute MI, dilated cardiomyopathy Others Causes: chronic CAD, electrolyte abnormalities, drug toxicities Monomorphic VT (MC): *regular, broad complex tachycardia *uniform QRS complexes within each lead (i.e., each QRS is identical) *usually associated w/ myocardial scar Polymorphic VT: *QRS morphology continuously varies (requires >1 EKG lead to see variation) *most often d/t ischemia in absence of QT prolongation Brugada Syndrome: hereditary, characterized by structurally normal heart *associated w/ ventricular dysrhythmias ⇢ syncope & sudden cardiac death – d/t mutation in cardiac Na gene channel (“sodium channelopathy”) *Asian men predominantly

Answer 7

S/SXS: CP, dyspnea, syncope, sudden cardiac death dx Monomorphic VT (MC): uniform QRS pattern, consistent morphology; rate 150-200bpm Polymorphic VT: QRS morphology continuously varies Brugada Pattern: pseudo-RBBB + persistent ST segment ⇡ (coved) in V1-V2 tx Unstable: assume VT *cardioversion Stable VT: IV amiodarone first line – DCC if VT fails to terminate/sxs worsen Polymorphic: IV magnesium Pulseless 🡪 ACLS Recurrent, refractory: overdrive pacing – Internal cardiac defibrillator (ICD)

Answer 8

*paroxysmal form of polymorphic VT *occurs secondary to QT prolongation, can be acquired (MC) or congenital Acquired QT Prolongation: – RX: haloperidol, TCAs, abx (e.g., macrolides), methadone, antihistamines, antiemetics, anticonvulsants – Electrolyte Abnormalities: hypokalemia, hypomagnesemia, hypocalcemia dx Torsades de pointes (“twisting of the points”): ▪︎paroxysmal form of polymorphic VT, sinusoidal; rates >200bpm tx *IV magnesium sulfate Unstable: DCC Refractory: ICD

Answer 9

*total disorganized ventricular depolarization *ventricle impulse rates up to 500bpm *total loss of synchronized ventricular contraction, complete loss of CO dx Ventricular Fibrillation: chaotic irregular zigzag pattern of varying amplitude ▪︎no identifiable P waves or QRS complexes, rates varying between 150-500bpm ▪︎as times passes, amplitude typically decreases (coarse ⇢ fine) tx ACLS Algorithm: – CPR, defibrillation – Epinephrine 1mg – Amiodarone

Answer 10

2 key features of both left & right BBBs: ➀ prolonged QRS duration ➁ terminal conduction delay ▪︎Complete BBB: QRS ≥120ms ▪︎Incomplete BBB: QRS 110-120ms Right Bundle Branch Block (RBBB): delay in depolarization of RV *CAN occur in a healthy heart Left Bundle Branch Block (LBBB): delay in depolarization of LV; entire sequence of ventricular activation is altered, affecting both the initial septal & subsequent ventricular forces *does NOT occur in a healthy heart dx RBBB: QRS ≥120ms ▪︎terminal R wave in V1/V2 (rSR’) w/ discordant ST/T waves » direct opposite of R’ (i.e., ST ⇣ or T wave inversion) ▪︎broad S waves in V5/V6 LBBB: QRS ≥120ms ▪︎broad, notched, or slurred R waves (rR’/RR’) in leads I, aVL, V5/V6 ▪︎dominant S wave in lead V1 ▪︎absence of Q waves in lateral leads, appropriate ST/T discordance tx Bundle Branch Blocks: ▪︎asymptomatic: no further tx ▪︎symptomatic: permanent pacemaker

Answer 11

Fascicular Blocks: partial blocks in left bundle system (i.e., left anterior or posterior fascicular blocks) ▪︎generally do not prolong QRS substantially but instead cause left/right axis deviation » Left Anterior Fascicular Block (LAFB): delay in depolarization of anterior & superior LV ▪︎QRS <120ms, LAD » Left Posterior Fascicular Block (LPFB): delay in depolarization of inferior & posterior LV ▪︎QRS <120ms, RAD dx LAFB: QRS <120ms, LAD (lead I⊕, aVF⊖) ▪︎qR complexes in leads I & aVL, rS complexes in leads II, III, & aVF LPFB: QRS <120ms, RAD (lead I⊖, aVF⊖) ▪︎rS complexes in leads I & aVL, qR complexes in leads II, III, & aVF tx Fascicular Blocks: no specific treatment ▪︎treat underlying disorder

Answer 12

MOA: slows conduction through the AV node via activation of adenosine-I receptors; ⇣ conduction velocity, ⇡ ERP Indications: rapid conversion to NSR in PSVT

Answer 13

MOA: blocks at AV node = ⇣ conduction velocity, ⇡ nodal ERP Indications: ventricular rate control in SVT; ineffective at controlling rate during exercise; used in combo w/ BB or CCB

Answer 14

Characterized by reduced strength of contraction & systolic dysfunction, results in right &/or left ventricular enlargement & progressive heart failure w/ increased risk for sudden cardiac death HF SXS: exertional dyspnea, fatigue, edema, cough, hepatomegaly PE: S3 gallop hallmark ▪︎cardiomegaly, elevated JVP, rales ▪︎mitral or tricuspid regurgitation dx ECHO: ▪︎left ventricular dilation, thin ventricular walls ▪︎⇣ EF, ventricular hypokinesis CXR: cardiomegaly, pulmonary edema, pleural effusion EKG: may show sinus tachycardia or arrhythmias tx HF TX: ACEI, BB, diuretics ▪︎automated implantable cardioverter/defibrillator if EF <35-30%

Answer 15

▪︎Autosomal dominant genetic disorder of inappropriate LV &/or RV hypertrophy w/ diastolic dysfunction ▪︎Subaortic outflow obstruction due to asymmetrical septal hypertrophy & systolic anterior motion of the mitral valve The obstruction worsens w/: ⇡ contractility (exercise, Digoxin, beta agonists) ⇣ LV volume (dehydration, ⇣ venous return, Valsalva) HF SXS: dyspnea MC, fatigue, angina, syncope, dizziness, arrhythmias; sudden cardiac death PE: harsh systolic murmur best heart at LLSB ⇡ intensity: ⇣ venous return (Valsalva, standing) ⇣ intensity: ⇡ venous return (squatting, supine, leg raise) handgrip (⇡ afterload) +/- loud S4, mitral regurgitation, or pulsus biferiens dx ECHO: ▪︎asymmetric ventricular wall thickness (esp. septal) ▪︎systolic anterior motion of the mitral valve ▪︎small LV chamber size EKG: LVH tx ▪︎BBs, CCBs, disopyramide ▪︎myomectomy, alcohol septal ablation *pts should avoid dehydration, extreme exertion, & exercise; cautious use of digoxin, nitrates, & diuretics

Answer 16

Diastolic dysfunction in a non-dilated ventricle, which impedes ventricular filling (⇣ compliance); stiff ventricle fills w/ great effort Etiologies: infiltrative diseases: amyloidosis MC, sarcoidosis, hemochromatosis sx: R-sided HF > L-sided HF ▪︎R-sided HF: peripheral edema, JVD, hepatomegaly, ascites, GI sxs ▪︎L-sided HF: dyspnea, fatigue ▪︎Kussmaul’s sign: ⇡ JVP w/ inspiration dx ECHO: ▪︎non-dilated ventricles w/ normal thickness ▪︎diastolic dysfunction ▪︎marked dilation of both atria tx: underlying issue

Answer 17

Transient regional systolic dysfunction of the LV that can imitate MI but is associated w/ absence of significant obstructive CAD or evidence of plaque rupture Risk Factors: postmenopausal women exposed to physical or emotional stress PATHO: thought to be multifactorial, including catecholamine surge during physical or emotional stress, microvascular dysfunction, & coronary artery spasm sx: Similar to ACS ⇢ substernal CP, dyspnea, syncope dx EKG: ST ⇡ (esp. in anterior leads); may have ST ⇣ Cardiac enzymes: often⊕ Coronary angiography: absence of acute plaque rupture or obstructive coronary disease ECHO: transient regional LV systolic dysfunction, esp. apical left ventricular ballooning; usually performed after ACS has been r/o tx Initial: ASA, NTG, BB, heparin, coronary angiography Short-term: conservative & supportive - BBs - ACEI for 3-6mo - serial imaging to assess for improvement - anticoagulation in some w/ severe LV dysfunction or if thrombus present

Answer 18

ACCF/AHA & HFSA: complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood leading to cardinal manifestations of dyspnea, fatigue, fluid retention *Chronic HF: pts w/ longstanding (e.g., months-years) s/sxs of HF *Acute HF: rapid onset or worsening of sxs of HF; most episodes result from worsening of chronic HF, but ~20% are due to new-onset HF that can occur in the setting of ACS, acute valvular dysfunction, hypertensive urgency, postcardiotomy syndrome

Answer 19

*HFrEF: EF ≤40% *HFmrEF: EF 40-50% *HFpEF: EF ≥50%

Answer 20

L-side sxs: pulmonary venous congestion (Lungs, L-sided) *dyspnea MC *exertional, orthopnea, paroxysmal nocturnal dyspnea *fatigue *rales/crackles (less likely in chronic HF) R-side sxs: systemic venous congestion (SVC, IVC, hepatic) *weight gain, lower extremity edema *abdominal bloating, anorexia, early satiety *RUQ pain w/ N/V *hepatomegaly, splenomegaly, ↑ JVP *hepatojugular reflux; ↑ JVP w/ liver compression PE: S3 gallop (+/- S4) *apical impulse displaced downward & to the left *+/- pulsus alternans Severe HF: anxious, diaphoretic, dyspneic, pallor, duskiness, cool extremities, cyanosis

Answer 21

NYHA Functional Classification: *Class I: no limitation of activity, ordinary activity does not cause symptoms *Class II: slight limitation; comfortable at rest, but ordinary activity causes symptoms *Class III: marked limitation; only comfortable at rest, less than ordinary activity causes symptoms *Class IV: symptoms at rest, unable to carry out any activity without symptoms

Answer 22

DX: suspect if 1+ s/sxs of HF w/ no apparent non-cardiac cause ECHO: assess LVEF *LVEF ≥50% 🡪 workup for HFpEF *LVEF <50% 🡪 workup for HFrEF BNP >100pg/mL NT-proBNP: *<50y: >450pg/mL *50-75y: >900pg/mL *>75y: >1800pg/mL EKG: can show AFIB, LA enlargement, LVH, pathologic Q waves CXR: findings of pulmonary edema *cephalization of pulmonary vessels *Kerley B lines *peribronchial cuffing *pleural effusions *cardiomegaly Hemodynamic exercise test: RHC w/ PCWP assessed at rest & w/ exercise *PCWP ≥15mmHg at rest *PCWP ≥25mmHg w/ exercise Labs: CMP, CBC, coagulation studies, UA *elevated BUN/Cr *hyponatremia, hypo/hyperkalemia *anemia

Answer 23

Lifestyle: smoking cessation, alcohol restriction, sodium ≤3g/d, fluid ≤1.5-2L/d, weight loss Guideline-Directed Medical Therapy (GDMT): *diuretic PLUS *ARNI, ACEI, or ARB PLUS *beta blocker Diuretic Therapy: typically loop diuretic *furosemide, torsemide ARNI: sacubitril-valsartan ACEI: if no hx of angioedema (“prils”) ARB: for pts that cannot take ARNI or ACEI (“sartan”) Beta blocker: carvedilol, metoprolol succinate, bisoprolol ISDN-hydralazine: alternative to angiotensin blockers (ARNI, ACEI, ARB) Secondary Therapy: *MRA (spironolactone, eplerenone): for pts who are symptomatic (stages II-IV) + have EF ≤35% on optimal initial pharmacologic therapy Other secondary therapies depend on indications: SGLT2-inhibitors, vericiguat, ivabradine, digoxin Acute HF: *loop diuretic: first line for volume overload w/ congestion *vasodilators: used for pulmonary congestion for rapid relief of dyspnea *IV NTG, sodium nitroprusside, nesiritide *inotropic therapy: used for hypotension *dobutamine, milrinone, dopamine *position: sit pt up, have legs dangle over bed to decrease preload/venous return; positive pressure (ventilation)

Answer 24

Mitral > aortic > (mitral & aortic) > tricuspid *IVDU = tricuspid PATHO: endocardial injury 🡪 focal adherence of platelets & fibrin 🡪 microorganisms circulating in blood infect platelet-fibrin nidus *mature vegetation is a collection of fibrin, platelets, leukocytes, RBC debris, & dense clusters of bacteria Acute: healthy hearts, rapidly progressive w/ high fevers, rigors, sepsis; S. aureus MCC Subacute: pre-existing heart disease, non-specific symptoms, indolent; viridans streptococci MCC Native Valve (NVE): S. aureus MCC, viridans strep, Enterococcus Prosthetic Valve (PVE): *<2mo: S. aureus, *CoNS, gram⊖ bacilli, Candida *2-12mo: CoNS, S. aureus, streptococci, enterococci *>12mo: streptococci & S. aureus, CoNS, enterococci *CoNS: S. epidermis MC IVDU: S. aureus MCC, unusual gram⊖, fungi *tricuspid valve

Answer 25

MC S/SXS: FEVER, MURMURS *chills, anorexia, weight loss, malaise, HA, *myalgias, arthralgias, night sweats *abdominal pain, dyspnea, splenomegaly *petechiae (palate, conjunctiva, extremities) *splinter hemorrhages Uncommon, but highly suggestive of IE: *Janeway lesions: NONTENDER erythematous macules on palms/soles *Osler nodes: TENDER nodules on finger/toe pads (“Osler, Ouch”) *Roth spots: exudative, edematous, hemorrhagic lesions of retina w/ pale centers Systemic complications at presentation: *cardiac – valve regurgitation, HF *neuro – embolic stroke, ICH, brain abscess *septic arterial or pulmonary emboli *vertebral osteomyelitis, septic arthritis *glomerulonephritis (hematuria, proteinuria)

Answer 26

Labs: ↑ ESR, mild anemia, +RF, leukocytosis w/ left shift *non-specific EKG: +/- new or evolving conduction disease (1st/2nd degree AV block, BBB, complete heart block) *consider perivalvular abscess if prolonged PR CXR: evaluate for presence of septic pulmonary emboli, infiltrate (w/ or w/o cavitation), CHF Blood cultures x3: different venipuncture sites, at least 1h between first & last, 3 sets ⊕>95% cases *repeat q48-72h until clearance of bacteria ECHO: ASAP (<12h after initial evaluation); TTE then TEE *TTE insensitive in PVE, use TEE *TEE superior for detecting complications (e.g., abscess, leaflet perforation, aortic pseudoaneurysm, fistula) Major Criteria: 2 positive blood cultures positive ECHO or new valvular regurg Minor RF: prosthetic valve, IVDU, valve lesion Fever greater than 100.4 vascular phenomena immunologic phenomena

Answer 27

Empiric antibiotic therapy warranted for any patient w/ signs of clinical instability Empiric Antibiotic Therapy (IV): NVE: Vancomycin + Ceftriaxone x4-6wks PVE: Vancomycin + Rifampin x6wks + Gentamicin for first 2wks *persistent fever after 1wk suggests a septic embolic focus or inadequate coverage *reappearance of fever after initial resolution suggests septic emboli or drug fever Common Surgical Indications: *refractory HF, myocardial abscess *valvular obstruction or dysfunction *perivalvular extension (new conduction dz) *persistent bacteremia, fungal endocarditis *recurrent emboli

Answer 28

High TC only = hypercholesterolemia High TGs only = hypertriglyceridemia High TC + TGs = hyperlipidemia Primary Causes: familial genetic disorders Secondary Causes: diabetes, alcohol, CKD, hypothyroidism, primary biliary cirrhosis/other liver disease, medications (e.g., thiazides, BBs, retinoids, antiretrovirals, cyclosporine, estrogen, steroids) Traditional ASCVD Risk Factors: HTN, diabetes, family hx of premature ASCVD, cigarette smoking, CKD, obesity Risk-Enhancing Factors: – family hx of premature ASCVD (M <55yo, F <65yo) – primary hypercholesterolemia (LDL ≥160mg/dL) – persistently elevated TGs ≥175mg/dL – CKD – metabolic syndrome – inflammatory disorders (e.g., RA, SLE, psoriasis, HIV) – high-risk race/ethnicity (e.g., South Asian ancestry) – hx of premature menopause (<40yo)

Answer 29

S/SXS: most are asymptomatic – High LDL 🡪 xanthomas *tendinous (e.g., Achilles, patellar, back of hand) *palmar (yellowish plaques), tuberous (located over joints) *eruptive (reddish papules all over body) – High LDL 🡪 xanthelasma (smaller than xanthoma) *yellow collection of cholesterol under skin, usually on/around eyelids – Hypertriglyceridemia *lipemia retinalis (cream-colored blood vessels in fundus) *pancreatitis (>500mg/dL) Screening Guidelines: determine if 1+ traditional RFs present & obtain baseline fasting lipid profile for individuals ≥20yo, reassess risk q4-6y *if 1+ traditional RF (HTN, obesity, diabetes, etc.): – f/u lipid screening at 25-30yo for males, 30-35yo for females *if Ø other traditional RF: – start regular lipid screening at 35yo for males, 45yo for female

Answer 30

TC: less than 200 TG: less than 150 HDL: greater than 50 F or 40 M LDL: less than 130 VLDL: 2-30

Answer 31

TX: lower LDL ▶︎ statins TX: lower triglycerides ▶︎ fibrates Initiate statin therapy for: 1) anyone w/ ASCVD (MI, stable/unstable angina, stroke, PAD, etc.) 2) anyone w/ LDL ≥190mg/dL 3) adults 40-75yo w/ ⊕diabetes regardless of LDL 4) adults 40-75yo w/ LDL 70-189mg/dL & ≥7.5% 10y ASCVD risk Treatment goals: – ≥50% LDL reduction for high-intensity statin – ≥30% LDL reduction for moderate-intensity statin Statin Therapy Monitoring: *baseline CK & aminotransferases, only repeat if sxs develop *repeat lipid profile 4-12wks after statin initiation/dosage change *monitor lipid profile q12mo thereafter *more frequent monitoring if concern for noncompliance

Answer 32

High Atorvastatin 40-80 mg Rosuvastatin 20-40 mg Moderate Atorvastatin 10-20 mg Rosuvastatin 5-10 mg Simvastatin 20-40 mg Pravastatin 40-80 mg Lovastatin 40 mg

Answer 33

MOA: inhibit the rate-limiting step in hepatic cholesterol synthesis via inhibition of the enzyme HMG-CoA reductase *increase LDL receptors, promoting LDL clearance; reduce triglycerides Indications: *best drug to decrease LDL *have been shown to decrease cardiovascular complications Muscle damage (myositis, rhabdomyolysis) ↑ LFTs, hepatitis GI sxs, DM Contraindications: active hepatic disease, persistent elevated LFTs, pregnancy/breastfeeding

Answer 34

2nd line for HLD MOA: increases HDL (delays HDL clearance); decreases hepatic production of LDL & its precursor VLDL; decreases triglycerides Indications: best drug to increase HDL levels Increased PGs (flushing, warm sensation, pruritis) *NSAIDs/aspirin can be given 30min before Dry skin, hyperuricemia, hyperglycemia Hepatotoxicity, GI (N/V, dyspepsia) Contraindications: active PUD, active liver disease, arterial bleeding

Answer 35

MOA: binds bile acids in the intestine, blocking enterohepatic reabsorption of bile acids; reduces cholesterol pool, lowers intrahepatic cholesterol *because the liver has to make new bile acids, it increases its LDL receptors, decreasing LDL levels Indications: often used in combo w/ statin to reduce LDL levels; mild to moderate increase in HDL *SAFE IN PREGNANCY *Cholestyramine used to treat pruritis associated w/ biliary obstruction

Answer 36

MOA: inhibits intestinal cholesterol absorption Indications: often used in combo w/ a statin to reduce LDL levels

Answer 37

*HTN associated w/ MI, HF, stroke, & CKD *↑ prevalence in ethnic minorities, ♀︎, & ↑ age Primary Essential HTN (MCC, 95%) *onset usually 25-50yo PATHO: sympathetic/RAAS overactivation, defect in natriuresis, variations in cardiovascular/renal development, ↑ intracellular Na/Ca levels Secondary HTN (5%), i.e., identifiable cause *suspect if HTN develops <25yo or >50yo *resistant to max doses of 3 drugs is another clue MCC: renal parenchymal disease

Answer 38

MC SXS: headache Fundoscopic exam: +/- hemorrhage, papilledema, cotton wool spots, arteriolar narrowing, AV nicking (hypertensive retinopathy) dx DX: BP ≥130/80 when averaged from 2+ readings obtained on 2+ occasions LABS: CBC, CMP (GFR, creatinine, Na/K/Ca), fasting blood glucose, lipid profile, uric acid, UA, TSH EKG: LVH tx Nonpharmacologic interventions: *weight loss, DASH diet, smoking cessation *salt restriction ≤1500mg/d (optimal) *potassium 3500-5000mg/d *aerobic exercise 90-150min/wk *≤2drink/d for men, ≤1drink/d for women Monotherapy vs Combination Drug Therapy: *stage 2 HTN & >20/10mmHg above goal – combo, fixed-dose combination preferred Initial TX w/ Monotherapy: *ACEI/ARB or CCB or thiazide-like diuretic Initial TX w/ Combo Therapy: *ACEI + DHP CCB single-pill combo – Amlodipine-Benazepril (Lotrel) – Perindopril-Amlodipine (Prestalia) F/u q4wks until BP controlled, then q3-6mo *if BP uncontrolled, escalate doses on current drugs to at least half max dose before adding additional agent Additional RX needed: – add agent from among 3 preferred classes *ACEI/ARB, CCB, thiazide-like diuretic

Answer 39

*BP ≥180/120, Ø signs of end-organ damage S/SXS: asymptomatic EXAM: should look for the s/sxs suggestive of end-organ damage *neuro sxs (e.g., seizures, vision changes, AMS), N/V, CP, tearing back pain, dyspnea *flame hemorrhages, exudates (cotton-wool spots), papilledema (fundoscopy) tx BP target <160/100, but MAP should not be lowered >25-30% over the first 2-4hrs, rapid lowering of BP can be harmful *Clonidine, Captopril, CCB, beta blocker, ACEI/ARB

Answer 40

*BP ≥180/120 + acute signs of end-organ damage “Malignant Hypertension” – encephalopathy or nephropathy + hypertensive retinopathy tx *IV Nicardipine (SBP ≥160), IV Labetalol (SBP <160) – Immediately reduce SBP <220 – Subsequent treatment over first 1-2h to ↓ SBP to 140-160

Answer 41

MOA: inhibit Na reabsorption in distal convoluted tubule, ↓ plasma volume, BP, & edema Indications: first-line agent, but ACEI/ARB or CCB generally preferred *useful in pts w/ osteoporosis or edema

Answer 42

MOA: cardioprotective, synergistic effect when used w/ thiazides; ↓preload/afterload, (↓ synthesis or AG II/aldosterone production), potentiates other vasodilators (bradykinin, PGs, NO); increases exercise tolerance; improves insulin’s actions Indications: first-line HTN agent (esp. for CKD, HFrEF, post-MI)

Answer 43

MOA: similar actions as ACEI but binds & blocks the angiotensin II receptor – does not increase bradykinin production Indications: first-line HTN agent, good for use in pts who cannot take ACEI

Answer 44

*large & medium vessel granulomatous vasculitis of the extracranial branches of the carotid artery (temporal artery, occipital artery, ophthalmic artery, posterior ciliary artery) sx *HA *jaw claudication w/ mastication *visual changes (anterior ischemic optic neuritis MC) +/- scalp tenderness Temporal artery 🡪 tender, pulseless, or normal Constitutional sxs: fever, fatigue, weight loss, night sweats, malaise dx Clinical Labs: *increased ESR & CRP *normocytic normochromic anemia Temporal biopsy – definitive tx: high-dose corticosteroids to prevent blindness (MC complication)

Answer 45

Inflammation of the heart muscle; MC in young adults PATHO: myocellular damage leads to myocardial necrosis & dysfunction, leading to HF Etiologies: *infectious: viral MC (enteroviruses – Coxsackievirus B) sx Viral prodrome – fever, myalgias, malaise for several days followed by sxs of systolic dysfunction (dilated cardiomyopathy) HF sxs: dyspnea, fatigue, exercise intolerance, S3 gallop dx CXR: cardiomegaly EKG: non-specific – sinus tachycardia MC Labs: may have + cardiac enzymes, ↑ ESR Echo: ventricular systolic dysfunction Endomyocardial bx: gold standard – infiltration of lymphocytes w/ myocardial tissue necrosis tx: Supportive

Answer 46

Inflammation of the pericardium, the outer layer of the heart Fibrinous or serofibrinous: e.g., post-MI, infectious Etiologies: *2 MCC – idiopathic, viral (Coxsackievirus & echovirus) *Dressler syndrome (post MI pericarditis + fever + pleural effusion) sx Chest pain: sudden onset *pleuritic (sharp, worse w/ inspiration) *persistent *postural (worse when supine & improved w/ sitting forward) *pain may radiate to back, shoulder, neck, arm, or epigastric area Pericardial friction rub: best heard at end expiration while upright & leaning forward dx EKG: diffuse ST elevations in the precordial leads w/ associated PR depressions in those leads tx Anti-inflammatory meds: NSAIDs or ASA x7-14d - colchicine second line Dressler Syndrome: ASA or colchicine - avoid NSAIDs because they can interfere w/ myocardial scar formation

Answer 47

Accumulation of fluid in the pericardial space sx *chest pain (if associated w/ acute pericarditis) *dyspnea, fatigue PE: decreased (muffled) heart sounds (due to fluid) dx Echo: test of choice – increased fluid in pericardial space EKG: electrical alternans (alternating amplitudes of the QRS complexes); low QRS voltage CXR: “water bottle” heart tx Treat the underlying cause (acute pericarditis) Serial echo if needed Large effusions may need pericardiocentesis for symptomatic relief

Answer 48

Pericardial effusion causing significant pressure on the heart, impeding cardiac filling, leading to decreased CO & shock sx Beck’s triad: *distant (muffled) heart sounds *↑ JVP *systemic hypotension Pulsus paradoxus: exaggerated (>10mmHg) ↓ in systolic pressure w/ inspiration Dyspnea, fatigue, peripheral edema, shock, reflex tachycardia, cool extremities dx Echo: pericardial effusion + diastolic collapse of cardiac chambers EKG: low voltage QRS complexes, electrical alternans CXR: may show enlarged cardiac silhouette Right heart catheterization: equalization of pressures in diastole tx IMMEDIATE PERICARDIOCENTESIS to remove the pressure - volume resuscitation & pressor support if needed - pericardial window drainage if recurrent

Answer 49

Loss of pericardial elasticity (thickening, fibrosis, calcification) leading to restriction of ventricular diastolic filling PATHO: fibrosis limits ventricular filling, decreased stroke volume & cardiac output sx *dyspnea (MC), fatigue, orthopnea Right-sided HF signs: *↑ JVD, peripheral edema, N/V *↑ hepatojugular reflex *Kussmaul’s sign (the lack of an inspiratory decline or an ↑ in jugular vein pressure w/ inspiration) Pericardial knock: high pitched diastolic sound similar to S3 (sudden cessation of ventricular filling) dx CXR: pericardial calcification may be seen esp. on lateral view, clear lung fields *normal or slightly increased heart size *square root sign on cardiac catheterization Echo: pericardial thickening &/or calcification (also used to r/o restrictive cardiomyopathy) *”square root” sign – early diastolic dip followed by a plateau if diastasis CT scan/MRI: pericardial thickening or calcification tx Diuretics for symptom relief as well as reduction of edema & venous pressure Definitive: pericardiectomy

Answer 50

Atherosclerotic disease of the arteries of the lower extremities sx Intermittent claudication – MC sxs (lower extremity pain w/ ambulation) *Leriche’s Syndrome: triad of buttock/thigh claudication + impotence + ↓ femoral pulses Ischemic rest pain: in advanced disease; MC at night & relieved w/ foot dependency PE: *pulses: decreased or absent; bruits (>50% occlusion), decreased capillary refill *skin: atrophic changes – muscle atrophy, thin/shiny skin, hair loss, thickened nails cool limbs, areas of necrosis; usually no edema LATERAL MALLEOLUS ULCERS *color: pale on elevation, dependent rubor (dusky red w/ dependency) dx ABI: most useful screening test *+ PAD if <0.90 (0.50 is severe); rest pain if <0.4 (normal is 1-1.2) *>1.2 🡪 possible noncompressible (calcified) vessels – may lead to a false reading Arteriography: gold standard – usually only performed if revascularization is planned tx Supportive: first line therapy – exercise (fixed distance walking), decreasing RF (smoking cessation associated w/ greatest benefit, hyperlipidemia, DM), foot care Platelet inhibitors: cilostazol most effective medical therapy; aspirin, clopidogrel, pentoxifylline Revascularization: percutaneous transluminal angioplasty (first line revascularization procedure) bypass grafts, endarterectomy (last line)

Answer 51

Acute limb ischemia – rapidly developing or sudden decrease in limb perfusion sx 6 Ps: paresthesias (often early), pain, pallor, pulselessness, poikilothermia, paralysis (late finding associated w/ a worse prognosis); sxs usually distal to the occlusion Decreased capillary refill, decreased or absent pulses, cool temperature dx Bedside arterial doppler to assess for pulses CT angiography or catheter angiography An immediately threatened limb may undergo further evaluation & treatment in a surgical suite tx Reperfusion mainstay of tx – surgical bypass, surgical or catheter based thromboembolectomy, endarterectomy; thrombolytic therapy or percutaneous angioplasty

Answer 52

*nonatherosclerotic inflammatory small & medium vessel vasculitis, leading to vasocclusive phenomena *suspect in young smokers/tobacco users w/ distal extremity ischemia/ischemic ulcers or gangrene of the digits sx Triad: distal extremity ischemia both upper & lower extremities (claudication in the lower calf or arch of the foot, ischemic ulcers), Raynaud’s phenomenon, & superficial migratory thrombophlebitis – due to decreased blood flow in the medium & small arteries and veins dx Abnormal Allen test: delayed perfusion of the radial ulnar arteries Aortography: corkscrew collaterals Biopsy: segmental vascular inflammation tx Smoking/tobacco cessation cornerstone of management Wound care—debridement, moist dressings, negative pressure wound therapy Amputation if gangrene occurs or to avoid the spread of infection in severe ischemic cases Iloprost: PG analog that may help w/ critical limb ischemia while smoking cessation is in progress CCBs for Raynaud’s phenomenon

Answer 53

*inflammation &/or thrombosis of a superficial vein *MC associated w/ IV catheterization, pregnancy, varicose veins, venous stasis sx Local phlebitis: tenderness, pain, induration, edema, & erythema along the course of the vein under the skin; may feel a palpable cord Trosseau sign: migratory thrombophlebitis associated w/ malignancy (e.g., pancreatic cancer); may be seen w/ other vasculitic disorders dx Mainly a clinical diagnosis Venous duplex U/S: noncompressible vein w/ clot & wall thickening Hypercoagulability workup: factor V Leiden (MC cause), prothrombin gene mutations, protein C & S, antiphospholipid antibodies, lupus anticoagulant, factor VII, homocysteine Migratory phlebitis: malignancy workup: carcinoembryonic antigen (CEA), prostate specific antigen (PSA), colonoscopy, CT scan, mammography (as indicated based on suspicion) tx Supportive mainstay – NSAIDs, extremity elevation, warm compresses Vein ligation/excision (phlebectomy): if extensive varicose veins, septic phlebitis, or persistent sxs despite supportive measures

Answer 54

Dilation of superficial veins due to failure of the venous valves in the saphenous veins, leading to retrograde flow, venous stasis, & pooling of blood sx Most are asymptomatic but may present due to cosmetic issues Dull ache or pressure sensation; pain is worse w/ prolonged standing or sitting w/ the leg dependent & is relieved w/ elevation PE: dilated visible veins, telangiectasias, swelling, discoloration, venous stasis ulcers: severe varicosities resulting in skin ulcerations; +/- mild ankle edema tx Conservative: compression stockings, leg elevation, pain control Ablation: catheter-based endovenous thermal ablation (laser or radiofrequency) Ligation & stripping, sclerotherapy

Answer 55

Changes due to venous HTN of the lower extremities as a result of venous valvular incompetency MC occurs after superficial thrombophlebitis, after DVT or trauma to the affected leg sx Leg pain worsened w/ prolonged standing, prolonged sitting w/ the feet dependent Leg pain improved w/ ambulation & leg elevation Pain classically described as a burning, aching, throbbing, cramping, or “heavy leg” PE: *stasis dermatitis: itchy eczematous rash (inflammatory papules, crusts, or scales), excoriations, weeping erosions & brownish or dark purple hyperpigmentation of the skin (hemosiderin deposition) *venous stasis ulcers MEDIAL MALLEOLUS ULCERS *dependent pitting leg edema, increased leg circumference, varicosities & erythema w/ normal pulse & temperature *atrophic blanche: atrophic, hypopigmented areas w/ telangiectasias & punctate red dots tx Conservative: initial management of choice – leg elevation, compression stockings, exercise, weight management Treat the underlying cause

Answer 56

*acute autoimmune inflammatory multi-systemic illness mainly affecting children 5-15yrs PATHO: *symptomatic or asymptomatic infectious w/ group A strep stimulates antibody production to host tissues & damages organs directly sx Polyarthritis *2 or more joints affected or migratory (lower 🡪 upper) *medium/large joints MC affected (knees, hips, wrists, elbows, shoulders) *heat, redness, swelling, & severe joint pain must be present *usually lasts 3-4wks Active carditis *can affect valves (esp. mitral/aortic), myocardium (myocarditis), &/or pericardium (pericarditis) Sydenham’s Chorea: “Saint Vitus Dance” may occur 1-8mo after initial infection *sudden involuntary, jerky, non-rhythmic purposeless movements esp. involving the head/arms Erythema marginatum: often accompanies carditis *macular, erythematous, non-pruritic annular rash w/ rounded, sharply demarcated borders (may have central clearing) *MC seen on trunk/extremities (not on face) Subcutaneous nodules: rare *seen over joints (extensor surfaces), scalp, & spinal column Other findings: abdominal pain, facial tics/grimaces, epistaxis dx JONES CRITERIA: 2 major OR 1 major + 2 minor MAJOR CRITERIA: *J – Joint (migratory polyarthritis) *O – Oh my heart (active carditis) *N – Nodules (subcutaneous) *E – Erythema marginatum *S – Sydenham’s chorea MINOR CRITERIA: Clinical *fever (≥101.3F) *arthralgia (joint pain) Laboratory *↑ ESR, CRP, leukocytosis *EKG: prolonged PR interval PLUS supportive evidence of a recent group A strep infection *⊕throat culture for GAS or *rapid streptococcal antigen or *⇡ streptococcal Ab titers (e.g., antideoxynuclease B or antistreptolysin O) tx Anti-inflammatory: *Aspirin (2-6wks w/ taper) +/- corticosteroids Complications: *rheumatic valvular disease (MC mitral/aortic)

Answer 57

Consequence of rheumatic fever characterized by inflammation & scarring of the heart valves *MC affects mitral valve > A > T Etiology: at least 1 episode of acute rheumatic fever from group A streptococci sx Early stage: valve regurgitation (MC mitral valve) Later stage: valve stenosis *early stage may last for years & may be asymptomatic *onset of sxs usually occurs 10-20yrs after acute rheumatic fever *palpitations, dyspnea, mitral regurgitation *mitral stenosis, aortic stenosis, aortic regurgitation dx Based on clinical presentation & confirmed w/ echo Echo: valvular abnormalities, including regurgitation or stenosis Labs: *↑ anti-streptolysin O (ASO) titers Histology: Aschoff bodies (granulomas w/ giant cells) on heart valves tx: Penicillin

Answer 58

Focal aortic dilation >1.5 normal (>3.0 considered aneurysmal) – infrarenal MC site Risk Factors: *smoking (main modifiable), >60yrs, Caucasians, males sx Most pts are asymptomatic – may be found incidentally on imaging or in pts w/ an abdominal bruit or a palpable abdominal mass Symptomatic (unruptured): *abdominal, flank, or back pain *on exam, an abdominal bruit may be auscultated & a palpable abdominal mass may be palpated Symptomatic (ruptured): *abdominal, flank, or back pain *abdominal bruit *pulsatile mass *hypotension or syncope *flank ecchymosis dx CT w/ contrast: best initial test in symptomatic, hemodynamically stable pts to deter presence, size, & extent Focused bedside U/S: may be initial study of choice in hemodynamically unstable pts w/ suspected AAA Pts w/ known AAA who present w/ classic sxs or signs of rupture can be taken to the operative room for surgical repair w/o preoperative imaging Asymptomatic w/ suspected AAA: *abdominal U/S: initial test in asymptomatic pts & to monitor progression tx Symptomatic or ruptured: *IMMEDIATE SURGICAL REPAIR -endovascular stent graft -open repair *BBs reduce shearing forces, decreases expansion & rupture risk AAA Screening: one-time screening via abdominal U/S in men 65-75yrs who ever smoked

Answer 59

Tear through the innermost layer of the aorta (intima) due to cystic medial necrosis Ascending MC near the aortic arch or left subclavian *descending *aortic arch Risk Factors: *HTN (most important) *age >50yrs *men, vasculitis, trauma, family hx *Turner’s syndrome *collagen d/o (Marfan, Ehlers-Danlos), pregnancy sx Chest pain: sudden onset severe, tearing (ripping, knife-like) chest/upper back pain; may radiate between the scapulae *ascending: anterior chest pain *aortic arch: neck/jaw pain *descending: interscapular pain Unequal BP in both arms dx CT angiogram, MR angiogram, TEE CXR: widened mediastinum tx Acute proximal: surgical - preoperative BP control Descending/distal: medical - non-selective BBs (labetalol) +/- sodium nitroprusside - SBP rapidly lowered to a goal of 100-120 within 20min

Answer 60

MC Prothrombotic States: *Factor V Leiden mutation *Prothrombin gene mutation Risk Factors: *hx of immobilization (e.g., travel) *recent surgery/trauma (~12wks) *previous VTE, family history of VTE *obesity, >65yo, malignancy, smoker *pregnancy, postpartum, OCPs, HRT *heart failure, IBD Provoked DVT: ⊕identifiable RF Unprovoked DVT: ⊖identifiable RF

Answer 61

sx S/SXS: LE swelling (unilateral), pain, warmth, & erythema *isolated distal DVT: symptoms confined to calf *proximal DVT: calf or whole leg symptoms *Homans’ sign (calf pain on passive foot dorsiflexion) is UNRELIABLE for presence of DVT dx D-dimer (✓sensitivity, ✗specificity) *useful to r/o DVT *high ⊖predictive value for low/moderate PTP DVT unlikely (low/moderate PTP) ⇢ D-dimer ⊖ = <500ng/mL ⇢ DVT ruled out, no further testing ⊕ = ≥500ng/mL ⇢ compression U/S w/ Doppler DVT likely (high PTP) ⇢ compression U/S w/ Doppler *NO D-DIMER FIRST Compression U/S w/ Doppler: ⊖ = full compressibility of all imaged veins ⊕ = non-compressibility of imaged vein w/ pressure Ascending contrast venography *CT/MR venography previously gold standard, now rarely used tx AC choice ⇢ DOACs *avoid use if CrCl ≤30 Proximal DVT ⇢ AC alone > thrombolytic + AC IVC filter only recommended if CI to AC Primary Treatment (at least 3mo) ➀ Provoked by transient/chronic RF, unprovoked ⇢ shorter AC course (3-6mo) recommended Secondary Prevention (after primary treatment) ➀ DC anticoagulation vs continue indefinitely

Answer 62

S1: closure of the mitral & tricuspid valves – comprised of M1 & T1: M1 is mitral valve closing, T1 is tricuspid valve closing S2: closure of the aortic & pulmonic valves – comprised of A2 (first) & P2 (second): A2 is aortic valve closing, P2 is pulmonic valve closing S2 splitting Physiologic: splitting of S2 into A2 & P2 w/ INSPIRATION – increased venous return to the right side of the heart delays the closure of the pulmonic valve (major effect), & decreased return to the left side of the heart speeds the closing of the aortic valve (minor effect) Ejection Click: MVP (chordae tendineae abruptly pulls the MV tight)

Answer 63

S3: vigorous LV filling – normal in pts <40yrs; >40 🡪 decreased LV contractility, myocardial failure, volume overload (Kentucky) after S2 S4: dull, low pitch sound caused by increased resistance to LV filling after an atrial contraction (no S4 in atrial fibrillation) Stiffening of the myocardium can occur from CAD, hypertension, cardiomyopathy, or aortic stenosis Opening Snap: opening of stenotic MV = MS; best heard at apex (Tennessee) before S1

Answer 64

Harsh/rumble sounds = think STENOSIS: AS, MS – abnormal forward flow of blood through (stenotic) valve that should be open; stenotic lesions lead to pressure overload; regurgitation leads to volume overload Blow sound = think REGURGITATION: AR, MR – abnormal backflow of blood (regurgitation) through an incompletely closed valve; regurgitation leads to volume overload

Answer 65

PATHO: LV outflow obstruction leads to a fixed CO, ↑ afterload, LVH, & eventually LV failure MC VALVULAR DISEASE – sxs usually occur when Aov <1cm2 sx Once symptomatic, lifespan is dramatically reduced *dyspnea *angina *syncope *CHF Systolic crescendo-decrescendo murmur *location: RUSB, radiates to carotid artery ↑ intensity: *sitting while leaning forward *↑ venous return (squatting, supine, leg raise) *expiration ↓ intensity: *↓ venous return (Valsalva, standing) *inspiration *handgrip (d/t ↓ ejection of blood) dx Echo: *small aortic orifice *LVH *calcified aortic valve tx Surgical therapy: replacement only effective treatment Percutaneous aortic valvuloplasty (PAV)

Answer 66

*right ventricular outflow obstruction of blood across the pulmonic valve Almost always congenital & a disease of the young (congenital rubella syndrome) sx Harsh mid-systolic crescendo-decrescendo murmur *location: LUSB, radiates to neck ↑ intensity: inspiration *longer murmur duration = ↑ stenosis *systolic ejection click (often buried in S1) *wide split S2 (delayed P2), +/- S4 dx: echo tx: Balloon valvuloplasty

Answer 67

Etiologies: *leaflet abnormalities: MVP MCC in US, rheumatic fever MCC in developing countries -endocarditis, valvulitis, LV dilation -Marfan syndrome *papillary muscle dysfunction sx Chronic: *HF sxs – dyspnea, fatigue *AFIB *hemoptysis, HTN Acute: *pulmonary edema *hypotension Blowing holosystolic murmur *location: apex, radiates to axilla ↑ intensity: *left lateral decubitus, expiration, exercise *↑ venous return (squatting, supine, leg raise) *handgrip ↓ intensity: *↓ venous return (Valsalva, standing) *inspiration, amyl nitrate dx Echo: *hyperdynamic LV, regurgitant jet EKG: nonspecific *left atrial enlargement, LVH *AFIB CXR: nonspecific *left atrial enlargement, LVH *pulmonary edema tx Medical: sxs control w/ afterload reducers or diuretics *ACEI, ARBs, hydralazine, nitrates Surgical: repair > replacement *indications: EF ≤60%, refractory to medical therapy

Answer 68

PATHO: right-sided pressure overload 🡪 right-sided HF Etiologies: *functional overload: pulm HTN, RV dilation *structural leaflet abnormalities: endocarditis, Ebstein anomaly sx Asymptomatic +/- pulsatile liver JVD Holosystolic, blowing, high-pitched murmur *location: L mid-sternal border ↑ intensity: *↑ venous return (squatting, supine, leg raise) *inspiration Carvallo’s Sign: ↑ intensity w/ inspiration *helps to distinguish TR from MR tx Medical: *diuretics (for volume overload & congestion) *LV dysfunction: standard HF therapy Surgical: suggested for pts w/ severe TR despite medical therapy *repair > replacement

Answer 69

*leaflets of the mitral valve bulge (prolapse) into the left atrium during systole *MVP MCC of MR in the US *MC in young women (15-35yrs) sx Most are asymptomatic Autonomic dysfunction: *anxiety, atypical chest pain *panic attacks, palpitations *syncope, dizziness, fatigue Mid-late systolic ejection click *location: apex dx Echo: posterior bulging leaflets w/ tissue redundancy tx Reassurance in most pts (good prognosis) Autonomic dysfunction: beta blockers Repair/replacement *reserved for MVP w/ severe MR to prevent CHF

Answer 70

Incomplete aortic valve closure leads to LV volume overload w/ eventual LV dilation & HF sx Signs of widened pulse pressure (seen in chronic) Water Hammer pulse: swift upstroke & rapid fall of radial pulse accentuated w/ wrist elevation Corrigan’s pulse (carotid) Hill’s sign (most sensitive) *popliteal > brachial BP by 60mmHg *bounding pulses, pulsus bisferiens Diastolic blowing decrescendo murmur *location: LUSB ↑ intensity: *sitting while leaning forward *↑ venous return (squatting, supine, leg raise) *expiration, handgrip ↓ intensity: *↓ venous return (Valsalva, standing) *inspiration, amyl nitrate Austin-Flint Murmur: mid-late diastolic rumble @ apex secondary to retrograde regurgitant jet competing w/ antegrade flow from LA into LV dx Echo: regurgitant jet Cardiac catheterization: definitive tx Medical therapy: afterload reduction *ACEI, ARBs, nifedipine, hydralazine Surgical: definitive *indications: acute or symptomatic, asymptomatic w/ LV decompensation (EF <55%)

Answer 71

PATHO: retrograde blood flow from pulmonary artery into RV 🡪 R-sided volume overload sx IF symptomatic: R-sided HF sxs Graham-Steell Murmur: brief decrescendo early diastolic murmur *location: LUSB w/ full inspiration *severe pulm. HTN ↑ velocity of regurgitation ↑ intensity: *↑ venous return (squatting, supine, leg raise) *inspiration ↓ intensity: *↓ venous return (Valsalva, standing) *expiration tx: No tx needed in most (well tolerated)

Answer 72

Blood backs up into the right atrium 🡪 increased right atrial enlargement 🡪 right sided HF sx Mid-diastolic murmur *location: LLSB ↑ intensity: *↑ venous return (squatting, supine, leg raise) *inspiration *opening snap (usually later than snap of MS) tx Medical: ↓ RA volume overload *diuretics *Na restriction Surgical: commissurotomy or replacement if R-HF or ↓ CO

Answer 73

PATHO: *obstruction of flow from LA to LV secondary to narrowed mitral orifice 🡪 blood backs up into the left atrium *↑ L-atrial pressure/volume overload 🡪 pulmonary congestion 🡪 pulmonary HTN 🡪 CHF Etiologies: *rheumatic heart disease almost always the cause – MC in 3rd/4th decade sx *dyspnea, hemoptysis *pulm. HTN *AFIB *enlarged atria *right-sided HF Mitral facies = flushed cheeks w/ facial pallor Ortner’s Syndrome: laryngeal nerve compression 🡪 hoarse Low-pitched, mid-diastolic rumbling murmur *location: apex *prominent S1, opening snap ↑ intensity: *left lateral decubitus, expiration, exercise *↑ venous return (squatting, supine, leg raise) ↓ intensity: *↓ venous return (Valsalva, standing) *inspiration dx EKG: *left atrial enlargement *AFIB *pulmonary HTN Echo CXR: left atrial enlargement Cardiac catheterization tx Percutaneous balloon valvuloplasty: *best tx for symptomatic MS in younger pts w/ noncalcified valves or if refractory to medical therapy Mitral valve replacement: reserved if mitral valvuloplasty is contraindicated or w/ unfavorable valve morphology Medical: *diuretics & sodium restriction for edema & volume overload *rate control of AFIB w/ BBs, CCBs, or digoxin (anticoag. for AFIB – warfarin)

Answer 74

Loss of Consciousness (LOC): a cognitive state of loss of awareness of self & situation w/ an inability to response to stimuli Transient Loss of Consciousness (TLOC): rapid onset, self-limited LOC w/ complete recovery Presyncope (near-syncope): prodromal symptoms of syncope (e.g., lightheadedness, N/V, diaphoresis, blurry vision) Syncope: transient, self-limited LOC caused by transient, self-terminating, inadequate nutrient flow to the brain Reflex Syncope (neurally-mediated): neural reflexes inappropriately modify HR & BP ▪︎Vasovagal syncope (VVS): » emotional stress (e.g., fear/pain, sight of blood) » orthostatic stress (e.g., prolonged standing, usually in a warm environment) ▪︎Situational syncope: coughing, swallowing, micturition/defecation ▪︎Carotid sinus syndrome/syncope (CSS): occurs w/ pressure on carotid sinus d/t carotid sinus hypersensitivity (CSH) » ⊕ = HR (ventricular) pause ≥3s &/or SBP ⇣ ≥50mmHg when pressure applied Orthostatic (postural) Hypotension (OH): SBP ⇣ ≥20mmHg or DBP ⇣ ≥10mmHg w/ upright posture ▪︎Medication-related: antidepressants (e.g., TCAs, phenothiazine APs), antihypertensive agents (e.g., β/⍺ blockers, hydralazine, ACEI), vasodilators (e.g., CCBs, nitrates), opiates, bromocriptine ▪︎Volume depletion: inadequate fluid intake, excessive loss (e.g., sweating, hemorrhage), vomiting/diarrhea ▪︎Autonomic failure » Primary: pure autonomic failure, multiple system atrophy, Parkinson » Secondary: diabetes, amyloidosis, spinal cord injuries, autoimmune neuropathy (Guillain-Barré) Cardiac: ▪︎Arrhythmias: tachyarrhythmias (e.g., VTACH, SVT), bradyarrhythmias (e.g., AV block, prolonged sinus pause) ▪︎Structural disease: severe aortic stenosis, HCM, cardiac tamponade, atrial myxoma ▪︎Cardiopulmonary/vascular: pulmonary embolism, acute MI/ischemia, severe pulmonary HTN, aortic dissection

Answer 75

Initial evaluation: detailed H&P, EKG, risk assessment, ECHO if structural heart disease suspected S/SXS: ▪︎Vasovagal ▪︎⊕prodromal SXS (e.g., dizziness, nausea, sweating) ▪︎clinical ▪︎recovery prompt but not immediate (5-15m) ▪︎precipitant apparent, reproducible ▪︎Orthostatic ▪︎SXS develop within several minutes of being upright ▪︎Arrhythmia ▪︎sudden onset w/o warning, unprovoked Dx ▪︎clinical +/- tilt table testing ⊕orthostatic vitals ▪︎Holter monitor ▪︎recovery immediate on awakening ▪︎may occur in any position ▪︎Structural ▪︎exertional syncope, prompt recovery ▪︎ECHO High risk arrhythmic causes: ▪︎persistent bradycardia <40bpm or sinus pauses >3s ▪︎3rd degree (complete) AV block ▪︎second degree, Mobitz II ▪︎pre-excited QRS complexes suggesting WPW ▪︎alternating L/RBBB ▪︎VT or PSVT w/ RVR ▪︎long or short QT intervals ▪︎Brugada syndrome

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